biopharmacological study on exposure to vegetable dusts in relation to b byssinosis

To clarify the role of different mediators which lead to the appearance of byssinotic symptoms, the changes in lung histamine content after manual inhalation of cotton and grain dusts were compared with those produced after i.p. administration of aqueous extracts of both dusts in guinea pigs. Calcium and magnesium ion concentrations in serum were estimated and correlated to the changes in histamine content after i.p injection of aqueous extract of cotton dust. Inhalation of both dusts manually vaporized did not produce any significant changes in histamine content of the lungs. The i.p. administration of grain dust caused no change in histamine content of lungs. Intraperitoneal injection of cotton dust extract did not produce any significant changes in magnesium ion concentration in the serum. It however produced a significant increase in calcium ion concentration after 4 weeks of injection

Drug-disease interactions II Salicylate interactions in rats with experimentally induced hepatotoxicity

Carbon tetrachloride induced hepatotoxicity caused a significant prolongation of prothrombin time probably due to its influence on vitamin K. Sodium salicylate caused a statistically significant prolongation of the prothrombin time in normal healthy rats as well as in rats with carbon tetrachloride induced hepatotoxicity. This may be attributed to the fact that liver damage prevents normal prothrombin formation. The hepatotoxic action of salicylate provides an explanation for the prothrombin time prolongation in salicylate- treated rats compared to untreated control rats. The statistically significant increase in the concentration of salicylate metabolites, salicyluric acid, salicylic acid, salicyl glucuronide, and total salicylate in the urine of hepatotoxic rats compared to normal rats can be explained by the influence of hepatotoxicity on the enzymes regulating metabolism and excretion of salicylates. Sodium salicylate aggravates the hepatotoxicity induced by carbon tetrachloride and this explains the decrease in its LD50 observed in the present work. The results of the present study may be of value in advising careful use of salicylates in patients suffering from liver damage

Pirenzepine and ranitidine as single agents and in combination in protection of the gastric mucosa against phenylbutazone injury

The protective effect of pirenzepine and/or ranitidine on phenylbutazone induced gastric ulcerations has been studied in the rat. Phenylbutazone produced severe gastric lesions in the glandular part of the stomach, which was accompanied with a significant increase in acid and pepsin. Pretreatment of the phenylbutazone treated rats with pirenzepine [100 mg/kg, X2 orally] significantly protected the rats and this was accompanied by significant lowering in acid and pepsin and a significant rise in the mucin content. While, pretreatment of the phenylbutazone treated rats with ranitidine [150 mg, X2 orally], also protected the animals against ulceration, but was accompanied with only a drop in acidity. Pretreatment of these animals with the drug combination [using only half of the dose of that used singly] afforded a higher protection ratio, a higher drop in acidity and pepsin and a marked rise in the mucin content. The data presented confirm the role of reduced acidity and peptic activity [aggressive factors] in the protection against phenylbutazone induced gastric lesions. It also emphasizes the necessity of giving preventive medications in the form of anti-ulcer agents when given anti inflammatory agents, bearing in mind the defensive factors involved. The study might also explain the synergistic anti-ulcer effect of the combined treatment with muscurinic M-blockers and histamine H2 blockers